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The Science Journal of the Lander College of Arts and Sciences

Abstract

In the past, the etiology of gout was simplistically believed to be based in the generous indulgence of rich foods and alcohol. However, research has revealed that gout has complex environmental and genetic origins. Specifically, researchers have begun to focus attention on the molecular basis of gout and its related features. These features include hyperuricemia, the stages of gout, and the decreased solubility of uric acid. Furthermore, with epidemiologic evidence indicating that the prevalence of gout is consistently rising, it is imperative that medical providers understand the research-based guidelines for treatment. This includes what medications to administer, monitoring for drug-induced adverse effects, and modifying the treatment plan in elderly or unresponsive patients. Medical providers must also be aware of the importance of diet as a contributing factor to gout and which foods increase or decrease the risk of gout. This review will, therefore, attempt to present the current understanding of the pathophysiology of gout and guidelines for treatment and dietary modifications. Because gout is a disease related to metabolic dysfunction and produces arthritic symptoms, the information presented in this review was extracted from textbooks and journals chiefly relating to biochemistry, rheumatology, and pharmacology. The results of the research conducted revealed that there are three features that are genetically induced that independently contribute to the onset of gout: phosphoribosyl pyrophosphate (PRPP) synthetase hyperactivity, partial deficiency of hypoxanthine-guanine phosphoribosyltransferase (HGPT), and hyperactivity of the uric acid transporter in the renal tubule. In addition, diets rich in meat and seafood and devoid of dairy products substantially increase the risk of developing gout. Finally, research has indicated that the preferred treatment plan for gout includes using NSAIDs to alleviate the pain and inflammation of an acute gout attack, using colchicine for prophylactic therapy, and using either uricosurics or xanthine oxidase inhibitors for the long-term management of uric acid levels. Based on the results presented, medical providers will be better informed of methods to treat gout by knowing how to skillfully manage drug therapy, thereby reducing dangerous adverse effects and improving patient adherence to the drug regimen. In addition, by understanding the role of diet in the onset of gout, providers will better be able to advise patients on what foods to include or limit in their diet. From a research perspective, the elucidation of the pathophysiology of gout can lead to the development of even more effective therapeutic options.

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